Gallium arsenide

Immunotoxicity

Description of key information

The reliable studies, especially the 14-week and 2-year inhalation toxicity studies with rats and mice, showed no immunotoxic action of GaAs and there are no hints for an immunotoxic action of GaAs.
The NTP inhalation toxicity studies revealed that GaAs causes a sort of local inflammation at the exposure site (lung) which is in line with the observed significant increase of the number of segmented neutrophils and is considered as a reaction of the immune system rather than a toxic action to the immune system. 
This is only true for inhalative exposure. Oral or dermal exposure to GaAs is tolerated without observable toxicity.

Additional information

There exist 29 not reliable studies or not assignable studies related to immunotoxicity of GaAs. Their results are ignored for the evaluation.

The results from fully reliable studies, especially the results of the 2-year inhalation toxicity studies with rats and mice, revealed that relatively low concentrations of GaAs in the air (i.e. 0.01 mg GaAs/m³) caused an inflammation in the lung after repeated exposure. Additionally in these studies a complete histopathology was performed on the lymph nodes (bronchial, mandibular, mediastinal, mesenteric), on the spleen and the thymus of all animals. No test article related effects were found in these organs.

Hematology data for immune system relevant cells such as the leukocytes (segmented neutrophils, lymphocytes, monocytes and eosinophils) were available for different GaAs concentrations in the the fully reliable 14-week inhalation studies on mice and rats (NTP, 2000). Except for the segmented neutrophils, no significant changes in the number of these cells have been observed after 14 weeks of GaAs exposure in female and male rat and mice. These data do not give a hint to any functional impairments of the immunsystem caused by GaAs. The observed significant increase of the number of segmented neutrophils is in line with the observed local inflammation at the exposure site (lung).

Hence, the reliable studies, especially the 14-week and 2-year inhalation toxicity studies with rats and mice, showed no immunotoxic action of GaAs.

Although in summary not reliable a study of Becker and McCoy (2003) seems to give in one part consistent results:

Becker and McCoy investigated in a ribonuclease protection assay 25 different cytokines of splenocytes and peritoneal residential cells. Mice were administered a single intraperitoneal dose of 200 mg GaAs/ kg bw.. At 6, 18, and 48 hours after exposure blood was collected, resident peritoneal leukocytes were harvested by lavage and splenic cell suspensions were prepared. Total RNA was prepared and analysed using the RiboQuant Multi-Probe Ribinuclease Protection Assay System. The MultiProbe assessed a panel of 25 different cytokines. 17 mRNA encoding for cytokines implicated in promoting inflammation and leukocyte taxis were detected at significantly higher levels than after vehicle treatment, while 3 anti-inflammatory cytokines were diminished to below detection limit. This set of experiments seems to show consistent results and supports the findings of the NTP inhalation toxicity studies that GaAs causes a local inflammation at the exposure site (lung). This is only true for inhalation exposure. Oral or dermal exposure to GaAs are tolerated without observable toxicity.

Justification for classification or non-classification

The reliable studies, especially the 2 -year study with rats and mice, showed no immunotoxic action of GaAs.